American Journal of Immunology

Correlation Between MMP-3, TIMP-3 Expression and Neuronal Apoptosis After Ischemia -Reperfusion Injury in Rates

Zi Xiaohong, Mutasem Abuhamed, Yuan Yi, Xu Haiqing, Lei Lifang, Guo Ke and Yang Qidong

DOI : 10.3844/ajisp.2007.25.30

American Journal of Immunology

Volume 3, Issue 2

Pages 25-30


Matrix metalloproteinases (MMPs) play a central role in many biological processes, such as embryogenesis, normal tissue remodeling, wound healing, and angiogenesis. How MMP3, TIMP3 expression and neuronal apoptosis (Fas, Fas-L and Bcl) may provide detrimental or beneficial actions during the injury and repair processes after cerebral ischemia-reperfusion injury in rates was studied. Adult rats underwent middle cerebral artery occlusion (MCAO) by the suture method. The expression of mRNA for TIMP-3, MMP-3, and neuronal apoptosis -were estimated in samples of Brain cortices of the ischemic penumbra (IPZ) and the core ischemic zone (ICZ) from70 Rates with Ischemic control group (ICG), 10 sham-operated group (SOG) and 60 Ischemic β-sodium aescinate intervention group (IβG) using the reverse-transcriptasepolymerase chain reaction with a synthetic multicompetitor standard. Also the amounts of neuronal apoptosis positive cells were evaluated by TUNEL assay. IβG expressed significantly TIMP-3, MMP-3 mRNA more than the ICG..Also in the ischemic zone Bcl-2 mRNA was strikingly increased whereas Fas and Fas-L mRNA was considerably decreased. At same time, the amount of apoptosis cells was maximally increased at 3 hours and was lowest decreased at 72 hours after reperfusion. Altogether, these results strongly suggest that inappropriate MMP-3 expression combined with increased TIMP-3, the ratio of apoptotic cells shows positive correlation with TIMP-3 , negative correlation with MMP-3 and MMP-3, TIMP-3 Expression might modulate the process of type I and type II neuronal apoptosis through FAS pathway.


© 2007 Zi Xiaohong, Mutasem Abuhamed, Yuan Yi, Xu Haiqing, Lei Lifang, Guo Ke and Yang Qidong. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.